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The Histone Methyltransferase MMSET Regulates Class Switch Recombination
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| Zeitschriftentitel: | The Journal of Immunology |
|---|---|
| Personen und Körperschaften: | , , , , , |
| In: | The Journal of Immunology, 190, 2013, 2, S. 756-763 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
The American Association of Immunologists
|
| Schlagwörter: |
| author_facet |
Pei, Huadong Wu, Xiaosheng Liu, Tongzheng Yu, Kefei Jelinek, Diane F. Lou, Zhenkun Pei, Huadong Wu, Xiaosheng Liu, Tongzheng Yu, Kefei Jelinek, Diane F. Lou, Zhenkun |
|---|---|
| author |
Pei, Huadong Wu, Xiaosheng Liu, Tongzheng Yu, Kefei Jelinek, Diane F. Lou, Zhenkun |
| spellingShingle |
Pei, Huadong Wu, Xiaosheng Liu, Tongzheng Yu, Kefei Jelinek, Diane F. Lou, Zhenkun The Journal of Immunology The Histone Methyltransferase MMSET Regulates Class Switch Recombination Immunology Immunology and Allergy |
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pei, huadong |
| spelling |
Pei, Huadong Wu, Xiaosheng Liu, Tongzheng Yu, Kefei Jelinek, Diane F. Lou, Zhenkun 0022-1767 1550-6606 The American Association of Immunologists Immunology Immunology and Allergy http://dx.doi.org/10.4049/jimmunol.1201811 <jats:title>Abstract</jats:title> <jats:p>Wolf–Hirschhorn syndrome (WHS) is a genetic disease with characteristic facial features and developmental disorders. Of interest, loss of the MMSET gene (also known as WHSC1) is considered to be responsible for the core phenotypes of this disease. Patients with WHS also display Ab deficiency, although the underlying cause of this deficiency is unclear. Recent studies suggest that the histone methyltransferase activity of MMSET plays an important role in the DNA damage response by facilitating the recruitment of 53BP1 to sites of DNA damage. We hypothesize that MMSET also regulates class switch recombination (CSR) through its effect on 53BP1. In this study, we show that MMSET indeed plays an important role in CSR through its histone methyltransferase activity. Knocking down MMSET expression impaired 53BP1 recruitment as well as the germline transcription of the Igh switch regions, resulting in defective CSR but no effect on cell growth and viability. These results suggest that defective CSR caused by MMSET deficiency could be a cause of Ab deficiency in WHS patients.</jats:p> The Histone Methyltransferase MMSET Regulates Class Switch Recombination The Journal of Immunology |
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The American Association of Immunologists, 2013 |
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The Journal of Immunology |
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| title |
The Histone Methyltransferase MMSET Regulates Class Switch Recombination |
| title_unstemmed |
The Histone Methyltransferase MMSET Regulates Class Switch Recombination |
| title_full |
The Histone Methyltransferase MMSET Regulates Class Switch Recombination |
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The Histone Methyltransferase MMSET Regulates Class Switch Recombination |
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The Histone Methyltransferase MMSET Regulates Class Switch Recombination |
| title_short |
The Histone Methyltransferase MMSET Regulates Class Switch Recombination |
| title_sort |
the histone methyltransferase mmset regulates class switch recombination |
| topic |
Immunology Immunology and Allergy |
| url |
http://dx.doi.org/10.4049/jimmunol.1201811 |
| publishDate |
2013 |
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756-763 |
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<jats:title>Abstract</jats:title>
<jats:p>Wolf–Hirschhorn syndrome (WHS) is a genetic disease with characteristic facial features and developmental disorders. Of interest, loss of the MMSET gene (also known as WHSC1) is considered to be responsible for the core phenotypes of this disease. Patients with WHS also display Ab deficiency, although the underlying cause of this deficiency is unclear. Recent studies suggest that the histone methyltransferase activity of MMSET plays an important role in the DNA damage response by facilitating the recruitment of 53BP1 to sites of DNA damage. We hypothesize that MMSET also regulates class switch recombination (CSR) through its effect on 53BP1. In this study, we show that MMSET indeed plays an important role in CSR through its histone methyltransferase activity. Knocking down MMSET expression impaired 53BP1 recruitment as well as the germline transcription of the Igh switch regions, resulting in defective CSR but no effect on cell growth and viability. These results suggest that defective CSR caused by MMSET deficiency could be a cause of Ab deficiency in WHS patients.</jats:p> |
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| author | Pei, Huadong, Wu, Xiaosheng, Liu, Tongzheng, Yu, Kefei, Jelinek, Diane F., Lou, Zhenkun |
| author_facet | Pei, Huadong, Wu, Xiaosheng, Liu, Tongzheng, Yu, Kefei, Jelinek, Diane F., Lou, Zhenkun, Pei, Huadong, Wu, Xiaosheng, Liu, Tongzheng, Yu, Kefei, Jelinek, Diane F., Lou, Zhenkun |
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| description | <jats:title>Abstract</jats:title> <jats:p>Wolf–Hirschhorn syndrome (WHS) is a genetic disease with characteristic facial features and developmental disorders. Of interest, loss of the MMSET gene (also known as WHSC1) is considered to be responsible for the core phenotypes of this disease. Patients with WHS also display Ab deficiency, although the underlying cause of this deficiency is unclear. Recent studies suggest that the histone methyltransferase activity of MMSET plays an important role in the DNA damage response by facilitating the recruitment of 53BP1 to sites of DNA damage. We hypothesize that MMSET also regulates class switch recombination (CSR) through its effect on 53BP1. In this study, we show that MMSET indeed plays an important role in CSR through its histone methyltransferase activity. Knocking down MMSET expression impaired 53BP1 recruitment as well as the germline transcription of the Igh switch regions, resulting in defective CSR but no effect on cell growth and viability. These results suggest that defective CSR caused by MMSET deficiency could be a cause of Ab deficiency in WHS patients.</jats:p> |
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| spelling | Pei, Huadong Wu, Xiaosheng Liu, Tongzheng Yu, Kefei Jelinek, Diane F. Lou, Zhenkun 0022-1767 1550-6606 The American Association of Immunologists Immunology Immunology and Allergy http://dx.doi.org/10.4049/jimmunol.1201811 <jats:title>Abstract</jats:title> <jats:p>Wolf–Hirschhorn syndrome (WHS) is a genetic disease with characteristic facial features and developmental disorders. Of interest, loss of the MMSET gene (also known as WHSC1) is considered to be responsible for the core phenotypes of this disease. Patients with WHS also display Ab deficiency, although the underlying cause of this deficiency is unclear. Recent studies suggest that the histone methyltransferase activity of MMSET plays an important role in the DNA damage response by facilitating the recruitment of 53BP1 to sites of DNA damage. We hypothesize that MMSET also regulates class switch recombination (CSR) through its effect on 53BP1. In this study, we show that MMSET indeed plays an important role in CSR through its histone methyltransferase activity. Knocking down MMSET expression impaired 53BP1 recruitment as well as the germline transcription of the Igh switch regions, resulting in defective CSR but no effect on cell growth and viability. These results suggest that defective CSR caused by MMSET deficiency could be a cause of Ab deficiency in WHS patients.</jats:p> The Histone Methyltransferase MMSET Regulates Class Switch Recombination The Journal of Immunology |
| spellingShingle | Pei, Huadong, Wu, Xiaosheng, Liu, Tongzheng, Yu, Kefei, Jelinek, Diane F., Lou, Zhenkun, The Journal of Immunology, The Histone Methyltransferase MMSET Regulates Class Switch Recombination, Immunology, Immunology and Allergy |
| title | The Histone Methyltransferase MMSET Regulates Class Switch Recombination |
| title_full | The Histone Methyltransferase MMSET Regulates Class Switch Recombination |
| title_fullStr | The Histone Methyltransferase MMSET Regulates Class Switch Recombination |
| title_full_unstemmed | The Histone Methyltransferase MMSET Regulates Class Switch Recombination |
| title_short | The Histone Methyltransferase MMSET Regulates Class Switch Recombination |
| title_sort | the histone methyltransferase mmset regulates class switch recombination |
| title_unstemmed | The Histone Methyltransferase MMSET Regulates Class Switch Recombination |
| topic | Immunology, Immunology and Allergy |
| url | http://dx.doi.org/10.4049/jimmunol.1201811 |